ART has improved the prognosis of HIV-infected patients, learn more resulting in a reduction in fibrosis progression and a decrease in liver disease-associated mortality. As mortality from AIDS has fallen, the importance of ESLD as a cause of significant morbidity and mortality in patients coinfected with HIV and HCV and/or HBV has become apparent, with hepatic complications accounting for more

than 80% of deaths [2–7]. HIV is associated with acceleration in liver disease progression to ESLD in those with HBV and/or HCV infection [8]. HCV/HIV infection is also associated with rapid deterioration after the development of cirrhosis, with a median survival after first episode of liver decompensation of 13 months compared with approximately 5 years in the HCV mono-infected patient [9].

The epidemic of acute hepatitis C in the HIV MSM population Bafilomycin A1 molecular weight has been associated with reports of rapid progression to cirrhosis with development of decompensated liver disease within 6 years [10]. Episodes of decompensation are associated with significant morbidity and mortality in HIV-infected patients [11]. Many cirrhosis-related complications and episodes of decompensation are avoidable. Patients need to be managed in conjunction with hepatologists or gastroenterologists who are experienced in the care of those with cirrhosis. Liver disease progression can be monitored by the application of simple and routinely available laboratory blood tests, which can be used in isolation or in combination to calculate prognosis risk scores, including the Child Pugh class and MELD score (Model for End-stage Liver Disease) (www.mdcalc.com/meld-score-model-for-end-stage-liver-disease-12-and-older and www.mdcalc.com/child-pugh-score-for-cirrhosis-mortality). Recent evaluation of HIV patients with ESLD has demonstrated Monoiodotyrosine that the MELD score is the best prognostic factor [12]. There is growing interest in the use of non-invasive

methods to diagnose disease stage and risk. Transient elastography may provide an estimate of risk for decompensation in HIV/HCV-infected patients [13] and may obviate the need for liver biopsy (see Section 4.3). Cirrhosis associated with chronic viral hepatitis coinfection is a well-recognised risk factor for the development of HCC which is seldom seen prior to the development of cirrhosis in HCV. HCV/HIV-infected patients develop HCC at a younger age and after a shorter duration than is observed for those with HCV-monoinfection, and survival may be shorter [14–17]. HBV is directly carcinogenic and is associated with the development of HCC prior to the development of cirrhosis, particularly in those where HBV has been acquired at birth or in early childhood [18]. High serum HBV DNA titre and low CD4 cell count have both been associated with an increased risk of development of HCC [19–20]. There are a number of treatment options for HCC.